Nutrition is an important consideration for the patient with respiratory insufficiency. The incidence of malnutrition is high, both in patients with chronic respiratory disease and those hospitalized with respiratory failure. Malnourished patients have an increased susceptibility to infection, a complication often resulting in mortality and morbidity in pulmonary patients. Nutritional support helps to meet the caloric needs for respiration and to maintain structure and function of respiratory muscle. In addition, the maintenance of nutritional status has been associated with an increased ability to wean patients from mechanical ventilatory support.
Published reports of respiratory failure precipitated by high-carbohydrate feedings have drawn attention to the carbohydrate and fat content of the patient's diet. In patients with chronic or acute retention of carbon dioxide (hypercapnia), one goal of dietary therapy is to decrease carbon dioxide production. High carbon dioxide production can precipitate acute respiratory failure in patients with chronic pulmonary disease and can complicate weaning in ventilator-dependent patients. Because the complete combustion of fat yields less carbon dioxide than combustion of either carbohydrate or protein, a high-fat diet may be preferable for patients with pulmonary disease.
Malnutrition is recognized as a major problem in hospitalized patients as well as in outpatients with chronic diseases of long duration. There is increasing evidence that patients with chronic obstructive pulmonary disease (COPD) and respiratory failure suffer from malnutrition. Symptoms of respiratory disease may limit caloric and nutrient intake, resulting in deterioration of nutritional status over time. Poor nutritional status, in turn, negatively affects pulmonary function.
The following observations are pertinent to the nutritional care of patients with lung disease:
(a) Weight loss occurs in 25% to 65% of patients as a result of inadequate caloric intake due to anorexia, shortness of breath, or gastrointestinal distress, or 2) increased caloric requirements due to the excess work of breathing; PA0 (b) In addition to having anthropometric abnormalities, these patients often have depressed biochemical measurements of nutritional status; PA0 (c) When caloric intake is decreased, the body cannibalizes muscles, including the respiratory muscles, to meet energy needs; PA0 (d) As a consequence of malnutrition, the energy content and strength of respiratory muscles decrease; PA0 (e) The degree of nutritional depletion is correlated with the severity of chronic lung disease; PA0 (f) In patients with chronic pulmonary disease, depressed nutritional status is associated with respitory failure and right heart failure (cor pulmonale); PA0 (g) Semistarvation depresses hypoxic ventilatory response; PA0 (h) Malnutrition lowers resistance to infection, which is a common complication in pulmonary disease; and PA0 (i) Improved nutritional status has been associated in an increased ability to wean from the respirator. PA0 (a) Increase fat consumption and decrease carbohydrate intake to reduce carbon dioxide production and lower the respiratory quotient; PA0 (b) Meet caloric requirements but do not exceed them, because overfeeding calories increases carbon dioxide production; PA0 (c) Avoid excessive protein intake because it may increase ventilatory drive in patients who have limited ability to respond; PA0 (d) Monitor fluid requirements, restricting fluid intake as needed for patients with heart failure; and PA0 (e) Provide adequate amounts of phosphorus, because acute hypophosphatemia may cause respiratory failure.
Patients with respiratory disease have specific nutritional needs. The goal of nutritional support is to provide required nutrients without further compromising respiratory, function. Although dietary management varies according to individual needs, the following dietary guidelines should be observed, especially for patients with hypercapnia:
Chronic obstructive pulmonary disease, chronic airway obstruction, and chronic obstructive lung disease are terms used to describe a group of disorders characterized by limitation of airflow in the lung and pulmonary insufficiency. Two disease entities that dominate the spectrum of disorders known as COPD are chronic bronchitis and pulmonary emphysema. Chronic bronchitis is characterized by excessive mucus secretion in the bronchial tree, with chronic or recurrent productive cough for two or more consecutive years. In emphysema, air spaces distal to the terminal bronchioles are enlarged, and their walls undergo destructive changes. Both these diseases result in obstruction of airflow, particularly during expiration.
Patients with COPD, which usually is a mixture of emphysema and chronic bronchitis, develop various degrees of respiratory muscle fatigue, hyperventilation, carbon dioxide retention (hypercapnia), and oxygen depletion (hypoxemia). Hypoxemia may cause constriction of the pulmonary arteries, resulting in increased pulmonary artery pressure. Chronic elevation of pulmonary artery pressure can cause episodes of cor pulmonale.
Hypoventilatory respiratory failure is recognized clinically when the partial pressure of carbon dioxide (PaCO.sub.2) is greater than 50 mm Hg and/or the partial pressure of oxygen (PaO.sub.2) is less than 50 mm Hg. In respiratory failure, the respiratory system does not provide sufficient oxygen to support body tissue metabolism, and carbon dioxide is not eliminated adequately through the lungs. The principal cause of hypoventilatory respiratory failure is COPD, the clinical course of which commonly includes exacerbations, usually caused by infections, trauma, or the inhalation of noxious fumes. Other causes of respiratory failure include interstitial lung disease, neuromuscular and chest wall dysfunction, depressed central ventilatory drive, carbon monoxide inhalation, and adult respiratory distress syndrome. Several studies report poor nutritional status in patients with respiratory failure.
As a result of reduced nutrient intake, body energy stores are depleted. The respiratory muscles, (diaphragmatic, intercostal, and accessory), like other skeletal muscles, are cannibalized to meet energy needs. Because work of the muscles stimulates protein synthesis and retards degradation, patients on prolonged mechanical ventilation, whose respiratory muscles move only passively, experience more atrophy than other patients. The decreased levels of energy-rich compounds in muscles, characteristic of malnutrition, are of special significance for patients with COPD and respiratory failure.
The symptoms of respiratory disease and malnutrition have a direct effect on the diaphragmatic muscle. Autopsy studies have shown that the weight of the diaphragm in persons with emphysema is decreased, and the decrease is proportionally greater than the reduction in total body weight. In addition to decreasing muscle mass, malnutrition causes a decrease in contractility of the diaphragm. Carbon dioxide retention also decreases the contractility and endurance time of the human diaphragm. Diaphragmatic weakness can contribute to respiratory failure.
Nutrition can affect central nervous system control of respiration. As opposed to normal individuals, in whom the drive to breathe is an increase in PaO.sub.2,the main ventilatory drive in patients with COPD and respiratory failure is hypoxia. Therefore, maintenance of hypoxic drive in these patients is important.
The relationship between nutrition and the immune system is well recognized. Poor nutritional status results in decreased resistance to infection. Malnourished individuals without chronic lung disease are particularly susceptible to pulmonary infection, which often is the immediate cause of death. Bacterial clearing from the lung is depressed by hypoxia and malnutrition.
Maintenance of the immune system is especially important for patients with COPD, since infection in the tracheobronchial tree is a common cause of respiratory failure in these patients. In many patients with COPD, a tracheostomy is performed as an alternative to repeated nasotracheal intubations. Colonization of the tracheobronchial tree with gram-negative enteric bacteria may occur subsequently.
The high prevalence of malnutrition among patients with advanced COPD and its correlation with anatomical and functional abnormalities, as well as mortality, suggest that nutritional care should be a part of therapy. There is increasing evidence that nutrition intervention can reverse the biochemical, anatomical, and functional abnormalities that have been described.
Marked weight loss has long been observed in patients with COPD. Insufficient caloric intake alone does not explain the observed weight losses. Even when patients with COPD have intakes equal to or greater than those of healthy, well-nourished individuals, weight loss and subnormal nutrition parameters are common. Malabsorption has been excluded as the primary cause of weight loss in these patients. These findings suggest that, in addition to decreased caloric intake, patients with COPD have enhanced caloric requirements, presumably due to the increased work of breathing.
It has been reported that weight loss and erosion of lean body mass tend to occur during acute exacerbations of the disease. Weight loss of 10% or more preceding heart failure has been reported in patients with COPD and hypercapnia. Also, mortality was significantly greater among the patients who lost weight. Nutritional repletion in patients with COPD results has been reported to result in improved respiratory function and quality of life.
The liquid nutritional product for enteral feeding of the present invention has been formulated to at least reduce the severity of the above described pulmonary related problems which are associated with nutrition.